ACK1 and BRK non-receptor tyrosine kinase deficiencies are associated with familial systemic lupus and involved in efferocytosis.
Stephanie GuilletTomi LazarovNatasha JordanBertrand BoissonMaria TelloBarbara CraddockTing ZhouChihiro NishiRohan BarejaHairu YangFrédéric Rieux-LaucatRosa Irene Fregel LorenzoSabrina D DyallDavid IsenbergDavid D'CruzNico LachmannOlivier ElementoAgnes VialeNicholas D SocciLaurent AbelShigekatzu NagataMorgan HuseW Todd MillerJean-Laurent CasanovaFrederic GeissmannPublished in: medRxiv : the preprint server for health sciences (2024)
Loss of function variants of human ACK1 and BRK kinase underlie systemic lupus erythematosus in young patients from multiplex families and disrupt the anti-inflammatory response of macrophages to apoptotic cells.
Keyphrases
- tyrosine kinase
- systemic lupus erythematosus
- inflammatory response
- epidermal growth factor receptor
- end stage renal disease
- endothelial cells
- disease activity
- ejection fraction
- induced apoptosis
- newly diagnosed
- chronic kidney disease
- cell death
- prognostic factors
- high throughput
- gene expression
- cell cycle arrest
- dna methylation
- lipopolysaccharide induced
- copy number
- endoplasmic reticulum stress
- lps induced
- pluripotent stem cells
- binding protein
- anti inflammatory
- real time pcr